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Slide Slam J5 Sandbox Series

FLAIR Enough: Identifying lesion and associated tissue damage and how this affects CBF and behaviour in post-stroke aphasia.

Slide Slam Session J, Wednesday, October 6, 2021, 5:30 - 7:30 pm PDT Log In to set Timezone

Kimberley Garden1, Veronika Vadinova1, Greig de Zubricay2, Marcus Meinzer3, Katherine O'Brien1, Tracy Roxbury1, Copland David1, Katie McMahon2, Sonia Brownsett1; 1University of Queensland, 2Queensland University of Technology, 3University Medicine Greifswald

Lesion volume is known to significantly correlate with motor, cognition, visual, and language impairments after stroke. However, the extent to which identified lesions includes white matter damage differs depending on whether the lesion is identified using T1 or FLAIR sequences. Perilesional tissue also plays a part in functional recovery, either in upregulation of residual networks or neurogenesis, when adequately perfused. Reduced cerebral blood flow (CBF) after stroke has been demonstrated in regions past the structural damage of a lesion and is associated with cognitive deficits. Given both the diffuse network involved in language, and the disparate regions involved in other cognitive networks known to contribute to language function under adverse conditions, CBF beyond perilesional areas should be considered when evaluating the contribution of any damage to recovery. Thus, this study aims to: 1) compare mean CBF within grey and white matter and grey matter only in regions surrounding stroke damage, 2) compare CBF between participants and controls, and 3) compare how CBF in these combinations differentially impacts on language performance in the early subacute stage of stroke recovery. Data from participants in the early subacute stage post-stroke and healthy controls underwent structural (high-resolution T1 and T2-FLAIR sequences) and perfusion (pseudo-continuous or pulsed arterial spin labelling; ‘PCASL’, ‘PASL’) imaging. Lesions were manually identified and reviewed using high-resolution T1 images, and additional associated stroke damage surrounding the lesion on the T2-FLAIR (‘lesionPLUS’). To assess CBF within regions surrounding lesion or lesionPLUS areas, lesions will be dilated in 3mm increments of adjacent rings. Individual grey matter only and grey plus white matter masks will be overlaid and mean CBF values from the left and right hemispheres will be extracted. Comparison of mean CBF between healthy controls and participants and mean CBF across hemispheres within participants will be conducted. Multiple linear regression analysis will be conducted to assess whether behavioural performance (spontaneous speech, naming and comprehension measures) are related to mean CBF values within the regions surrounding damage caused by the stroke beyond the lesion itself. The results from this study can potentially demonstrate how altered post-stroke perfusion influences language recovery. Additionally, it may inform functional neuroimaging studies regarding absence of activations in peri-damaged regions post-stroke.

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